Abstract：【Objective】To explore the effects of emodin on the expression of cytochrome C, bcl-2, PI3-K/Akt and ERK signaling pathways in inflammatory model of intestinal epithelial cell Caco-2.【Methods】A lipopolysaccharide (LPS)-induced Caco-2 inflammatory cell model was established and treated with different concentrations of emodin. The apoptosis, phosphorylation of Akt and ERK, cytochrome C and bcl-2 protein expression in Caco-2 cells before and after different concentrations of emodin treatment were compared.【Results】After induction of Caco-2 cells by LPS for 24 h, the apoptosis of Caco-2 cells was increased compared to vehicle control cells. Meanwhile the expression of cytochrome C was increased, and the expression of bcl-2 protein was decreased. After treatment with different concentrations of emodin for 24 h in LPS-induced Caco-2 cells, cell apoptosis was inhibited, cytochrome C expression decreased with increasing emodin concentration, and bcl-2 protein expression increased. Pretreatment with phosphatidylinositol kinase (PI3K) inhibitor LY294002 and extracellular signal-regulated kinase (ERK1/2) PD98059 reversed the inhibition of apoptosis by emodin, while increasing cytochrome C expression and decreasing the expression of bcl-2 as well. Also, emodin treatment inhibited the phosphorylation of Akt and ERK.【Conclusion】In the inflammatory model of intestinal epithelial cell line Caco-2, emodin inhibits cell apoptosis by regulating PI3-K/Akt and ERK signaling pathways through inhibiting phosphorylation of Akt and ERK. Emodin also reduced the expression of apoptotic cytochrome C and enhanced the expression of bcl-2.
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2019, Vol. 36 
